ArticleCell cycle (Georgetown, Tex.)2020
MicroRNA-23a-3p improves traumatic brain injury through modulating the neurological apoptosis and inflammation response in mice.
Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 42 citations in OpenAlex.
- Therapeutic potential of alpha-tocopherol in reducing oxidative stress and inflammatory damage after experimental traumatic brain injury and pentylenetetrazol-induced seizures.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Development of aBioactive materials · 2026Article
- Predominant miRNAs in Animal-Source Foods and Bioinformatic Analysis.Current issues in molecular biology · 2026Article
- The mechanisms by which hypothalamic neuroinflammation induced by neonatal cerebral ischemia-hypoxia leads to decreased thymic function via the HPA axis.Cell & bioscience · 2026Article
- Ozone Treatment Attenuates Neuroinflammation and Alters miRNA Expression in a Rat Model of Post-Traumatic Epilepsy.Neurochemical research · 2026Article
- Role of microRNAs in major brain diseases, focusing on neuroinflammation and neuronal apoptosis.Iranian journal of basic medical sciences · 2026Review
- Article
- Unveiling the predictive power of biomarkers in traumatic brain injury: A narrative review focused on clinical outcomes.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2025Review
- The Application of MicroRNAs in Traumatic Brain Injury: Mechanism Elucidation and Clinical Translation.Molecular neurobiology · 2025Review
- Potential Correlation Between Molecular Biomarkers and Oxidative Stress in Traumatic Brain Injury.International journal of molecular sciences · 2025Review
- Article
- Human Schwann Cell-Derived Extracellular Vesicle Isolation, Bioactivity Assessment, and Omics Characterization.International journal of nanomedicine · 2025Article
- Article
- Role of miRNAs in neurovascular injury and repair.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Review
- Analysis of miRNA Expression Profiles in Traumatic Brain Injury (TBI) and Their Correlation with Survival and Severity of Injury.International journal of molecular sciences · 2024Article
- Loss of microRNA-15a/16-1 function promotes neuropathological and functional recovery in experimental traumatic brain injury.JCI insight · 2024Article
- Identification of MicroRNA Profiles in Fetal Spina Bifida: The Role in Pathomechanism and Diagnostic Significance.International journal of molecular sciences · 2024Article
- Role of regulatory non-coding RNAs in traumatic brain injury.Neurochemistry international · 2024Review
- Role and regulatory mechanism of microRNA mediated neuroinflammation in neuronal system diseases.Frontiers in immunology · 2023Review
- The Role of Apoptosis and Autophagy in the Hypothalamic-Pituitary-Adrenal (HPA) Axis after Traumatic Brain Injury (TBI).International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secondary brain damage plays an important role in Traumatic brain injury (TBI) and inhibition of this damage has benefit for TBI treatment. However, the pathogenesis of secondary brain damage remains largely unknown. Here, we tried to explore the influence of microRNAs (miRNAs) on neuron apoptosis and inflammatory response after TBI. Firstly, the miRNA expression profiles were analyzed in the cerebral cortex tissues from the TBI mice model (controlled cortical impact) using miRNA microarray. miR-23a-3p (miR-23a) attracted our attention as its suppressive effects on apoptosis and inflammation. The further results showed that miR-23a upregulation improved long-term neurological function, the neuron apoptosis, and inhibited neuroinflammation, whereas knockdown of miR-23a had an opposite result. Using etoposide-induced primary cortical neurons injury model, we found that miR-23a was decreased in this cell model and miR-23a overexpression-suppressed etoposide induced the activity of caspase 3 and the releases of inflammatory mediators in primary cortical neurons. Phosphatase and tensin homolog (PTEN), a well‑known regulator of the AKT/mTOR pathway, was found to be a direct target of miR‑23a in the primary cortical neurons. Most importantly, it was found that miR-23a overexpression reactivated the AKT/mTOR pathway in TBI mice model, as demonstrated by the upregulation of phosphorylated (p‑)AKT and p‑mTOR. Taken together, these data indicate that miR-23a may serve as a therapeutic target for the treatment of TBI.
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